Common Regulatory Targets of NFIA, NFIX and NFIB during Postnatal Cerebellar Development

Fraser, James A.; Essebier, Alexandra; Brown, Allan H.; Davila, Raul Ayala; Harkins, Danyon; Zalucki, Oressia; Shapiro, Lauren P.; Penzes, Peter; Wainwright, Brandon J.; Scott, Matthew P.; Gronostajski, Richard M.; Bodén, Mikael; Piper, Michael; Harvey, Tracey J.

doi:10.1007/s12311-019-01089-3

Cited by 30 publications

(25 citation statements)

References 49 publications

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“…(A) Analysis of the Neurod2 locus using JASPAR (Fornes et al, 2020) identifies multiple Nfi transcription factor binding motifs (top). Analysis of Nfia, Nfib and Nfix ChIP-Seq data from the mouse cerebellum (Fraser et al, 2020) confirms binding of all three TFs to these motifs (bottom).…”

Section: Resultsmentioning

confidence: 89%

“…Both in-vitro and in the developing spinal cord, Neurod2-positive neurons are born after Nfia and Nfib expression commenced in progenitors(Delile et al, 2019) (compare Figures 4B and 5E). Motif analysis(Fornes et al, 2020) revealed multiple Nfi motifs in close proximity to the Neurod2 gene and analysis of recently published Nfia, Nfib and Nfix ChIP-seq datasets from the murine cerebellum(Fraser et al, 2020) confirmed binding of all 3 TFs to these sites (Figure 7A). We thus focused on assaying Neurod2 expression to determine the importance of Nfia and Nfib for the generation of late-born neurons in our in-vitro cultures.…”

mentioning

confidence: 81%

“…neurons (see also Figure S6) (A) Analysis of the Neurod2 locus using JASPAR (Fornes et al, 2020) identifies multiple Nfi transcription factor binding motifs (top). Analysis of Nfia, Nfib and Nfix ChIP-Seq data from the mouse cerebellum (Fraser et al, 2020) confirms binding of all three TFs to these motifs (bottom). (B,C) Neurod2 intensity histograms in control (B) and Nfia; Nfib double mutant (C) neurons at D11 in ventral conditions.…”

Section: Alignment Of Nfia/b/x Chip-seq Datamentioning

confidence: 94%

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Temporal patterning of the central nervous system by a shared transcription factor code

Sagner

Zhang

Watson

et al. 2020

Preprint

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The molecular mechanisms that ensure the reproducible generation of neuronal diversity in the vertebrate nervous system are incompletely understood. Here we provide evidence of a temporal patterning program consisting of cohorts of transcription factors expressed in neurons generated at successive developmental timepoints. This program acts in parallel to spatial patterning, diversifying neurons throughout the nervous system and in neurons differentiated in-vitro from stem cells. We demonstrate the TGFβ signalling pathway controls the pace of the temporal program. Furthermore, targeted perturbation of components of the temporal program, Nfia and Nfib, reveals their requirement for the generation of late-born neuronal subtypes. Together, our results provide evidence for the existence of a previously unappreciated global temporal program of neuronal subtype identity and suggest that the integration of spatial and temporal patterning programs diversifies and organises neuronal subtypes in the vertebrate nervous system.

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Section: Resultsmentioning

confidence: 89%

mentioning

confidence: 81%

Section: Alignment Of Nfia/b/x Chip-seq Datamentioning

confidence: 94%

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Temporal patterning of the central nervous system by a shared transcription factor code

Sagner

Zhang

Watson

et al. 2020

Preprint

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“…For example, the Nuclear Factor One (NFI) transcription factors regulate fetal muscle gene expression [ 1 ], retinal development [ 2 ], and dorsal telencephalic formation [ 3 , 4 ]. NFIX specifically promotes neural stem cell differentiation within the developing neocortex, hippocampus and cerebellum [ 5 – 8 ], as well as within the adult forebrain neurogenic niches [ 9 , 10 ]. Mechanistically, NFIs have been shown to drive differentiation within the nervous system via the activation of lineage-specific gene expression patterns, as well as via the repression of stem cell self-renewal genes [ 11 , 12 ].…”

Section: Objectivementioning

confidence: 99%

“…Finally, our data alone do not enable us to discern direct versus indirect targets of NFIX. This could be addressed in future using approaches such as chromatin immunoprecipitation and sequencing, which we have recently used to parse the roles of different NFI proteins within the postnatal cerebellum [ 5 ].…”

Section: Limitationsmentioning

confidence: 99%

Alterations in gene expression in the spinal cord of mice lacking Nfix

et al. 2020

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Objective Nuclear Factor One X (NFIX) is a transcription factor expressed by neural stem cells within the developing mouse brain and spinal cord. In order to characterise the pathways by which NFIX may regulate neural stem cell biology within the developing mouse spinal cord, we performed an microarray-based transcriptomic analysis of the spinal cord of embryonic day (E)14.5 Nfix−/− mice in comparison to wild-type controls. Data description Using microarray and differential gene expression analyses, we were able to identify differentially expressed genes in the spinal cords of E14.5 Nfix−/− mice compared to wild-type controls. We performed microarray-based sequencing on spinal cords from n = 3 E14.5 Nfix−/− mice and n = 3 E14.5 Nfix+/+ mice. Differential gene expression analysis, using a false discovery rate (FDR) p-value of p < 0.05, and a fold change cut-off for differential expression of > ± 1.5, revealed 1351 differentially regulated genes in the spinal cord of Nfix−/− mice. Of these, 828 were upregulated, and 523 were downregulated. This resource provides a tool to interrogate the role of this transcription factor in spinal cord development.

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PIN1 is a novel interaction partner and a negative upstream regulator of the transcription factor NFIB

Saritas Erdogan,

Yilmaz,

Kumbasar

2024

FEBS Letters

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NFIB is a transcription factor of the Nuclear Factor One (NFI) family that is essential for embryonic development. Post‐translational control of NFIB or its upstream regulators have not been well characterized. Here, we show that PIN1 binds NFIB in a phosphorylation‐dependent manner, via its WW domain. PIN1 interacts with the well‐conserved N‐terminal domains of all NFIs. Moreover, PIN1 attenuates the transcriptional activity of NFIB; this attenuation requires substrate binding by PIN1 but not its isomerase activity. Paradoxically, we found stabilization of NFIB by PIN1. We propose that PIN1 represses NFIB function not by regulating its abundance but by inducing a conformational change. These results identify NFIB as a novel PIN1 target and posit a role for PIN1 in post‐translational regulation of NFIB and other NFIs.

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Common Regulatory Targets of NFIA, NFIX and NFIB during Postnatal Cerebellar Development

Cited by 30 publications

References 49 publications

Temporal patterning of the central nervous system by a shared transcription factor code

Temporal patterning of the central nervous system by a shared transcription factor code

Alterations in gene expression in the spinal cord of mice lacking Nfix

PIN1 is a novel interaction partner and a negative upstream regulator of the transcription factor NFIB

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